GRC spoke with Dr. Shane Smith, one of the co-authors of the article that came out last July noting the numerous inaccuracies in the content and references of the Prentice List of 65 Purported Adult Stem Cell Therapies. Here's what he had to say about the Parkinson's community.

I really do think that the Parkinson community should be applauded for being early and vociferous supporters of stem cell research. I was personally impressed with your community’s level of organization and commitment and the level of savvy of individual advocates. For example, I can start a conversation about Parkinson's or stem cell research with a pd advocate using words like GDNF, cell differentiation, dopaminergic neuron and I don't always have to start from the basics. I think there are a number of communities who deserve a lot of credit for promoting stem cell issues, but advances in stem cell research should be a real indicator of success for the Parkinson community.

The interview on Grassroots Connection

http://grassrootsconnection.com/vip_shanesmith.htm

Paula

"The Truth About Adult Cell Therapy" is that it does not have any scientific basis when used for idiopathic Parkinson's Disease. For stem cells to be able to effectively treat idiopathic Parkinson's Disease there would need to be considerable loss of the dopaminergic neurons (the cells involved in Parkinson's Disease). Although this is widely claimed to be the case, not a single study has ever shown this.

This myth originated from a study carried out by Hornykiewicz in which it was claimed after carrying out autopsies on people with Parkinson's Disease that there was massive loss of the dopaminergic neurons.

However, the methods used did not even measure cell loss. As often occurs in published medical research, the conclusions did not match the methods or results. The methods used assessed the enzyme activity in people with Parkinson's Disease. Enzymes determine the acivity of the cells. So what they actually found was, in idiopathic Parkinson's Disease, that there was considerable lossof cell activity rather than considerable loss of cells.

Unfortunately hardly anyone bothers to read the full details of medical research. So the false conclusions in the abstract were able to persist.

Further research claimed to confirm the considerable cell loss theory. However, the methods they used were the f-Dopa PET scan. The f-Dopa PET scan doesn't measure cell loss either. It assesses cell activity.

Why has this myth persisted ?

Probably three reasons :

1. the medical establishment needs an excuse for all its big profit making wonder drugs not working. A basic knowledge of biochemistry would have made it obvious from the outset that they never could anyway. So they falsely claim that it is all due to masive cell loss - something that is beyond their control. Of course they didn't claim thisbefore they marketed their supposed wonder drugs.

2. wishful thinking by people that desperately need a solution to a potentially devastating disorder

3. this view has become the majority view. Why dsipute something you want to be true when so many people believe it ?

I have no doubt that people will continue to believe the myth of stem cells. However, time will prove the myth of the efficacy of stem cell therapy in idiopathic Parkinson's Disease to be only that. In the meantime, so much wasted discussion, effort and wishful thinking will take place because the complete lack of scientific basis has been persistently overlooked.

In anticipation of somebody claiming that I am writing this because I have some religious or ethical objections to the use of stem cells, I am a lifelong atheist and have no ethical views on the subject whatsoever.

But then, why should you listen to a cartoon duck anyway, even though it's true ?

for starting my day off on a positive note. Positive because I choose to believe that those D cells are dormant - or something like that - rather than dead. I also think that it is the drugs we resort to that cause most of the damage to those cells over time. I can't prove anything at this point but I'm trying to be living proof of this - in time - by recovering. Of course if/when that happens, "they" will say I didn't have pd, was misdiagnosed. Who cares? It'll just be an all but invisible error on the records of the 3 neurologists who have treated (prescribed drugs) me for PD.

As for ESCR, tho' I don't expect it to benefit me or other pd'ers, let's hope some good will come of it for something. I have a good friend who's been a parapalegic since age 17. Surely enabling him walk to again would justify using an embryo on it's way to the landfill - even if it does pad the wallets of the white coated researchers.

DD, what was that about the enzymes regarding dopamine use? I'm bio-chemically ignorant - but curious. Can you explain - or direct me to info? Thanks. Ibby

An enzyme is a chemical that enables a chemical reaction to take place in the body. Given that there are thousands of chemical reactions taking place in the body, enzymes are what keep people functioning properly.

Dopamine is made via the following means :

L-tyrosine >>> L-dopa >>> dopamine

One enzyme turns L-tyrosine in to L-dopa

A second enzyme turns L-dopa in to dopamine

It was these two enzymes that were found to be deficient in idiopathic Parkinson's Disease. Their activity in Parkinson's Disease drops to about 10% (in severe cases) and 30% (in milder cases) of what they should be. As they don't work properly, people don't produce enough dopamine.

It is loss of cell activity that is the problem. The cells are there. They just aren't working at a fast enough rate.

So, DD, what, specifically, are those enzymes?

If what you say is so, then wouldn't supplying those enzymes help in D production?

It just seems logical....

The enzyme that turns L-tyrosine in to L-dopa is tyrosine 3-monooxygenase (commonly called tyrosine hydroxylase).

The enzyme that turns L-dopa in to dopamine is L-aromatic amino acid decarboxylase (commonly called dopa decarboxylase).

In order to increase the levels of these enzymes, or in fact virtually any enzyme, you can not correct the problem by consuming them because enzymes are broken down as they enter the body.

The suspense is killing me, or maybe the PD

What can we consume to aid in the production of those enzymes?

Makes sense to me. The cells are there but they aren't doing enough. Then we take Sinemet-ie. dopamine which is the end result of this enzymatic cycle so the body senses that we don't need to produce as much of the enzyme and 'round we go....This brings another question to mind. Aren't enzymes protein based? Why would proteins block the uptake of the Sinemet. Can we help replace these enzymes by taking amino acids? Time to get out the chemistry books...

On another thread Rick writes of protein and coenzymes being needed to produce dopamine.

To be more specific, L-tyrosine is needed to stimulate the enzyme that makes L-dopa. L-tyrosine is normally obtained in high protein foods. The coenzymes that Rick mentions are made from vitamins.

A cofactor (in this case iron) is also essential for L-dopa formation. The Birkmayers showed that 110 out of 110 people that were supplemented with iron reduced their PD symptoms.

Ironically, no substance reduces L-dopa formation than L-dopa itself. That is why Sinemt can both relieve and also eventually cuse symptoms.

It's correct that enzymes are proteins. However, high protein foods can block Sinemet for other reasons.

Protein is made up of 20 different amino acids. Some of those amino acids are very similar to L-dopa. Consequently they compete with L-dopa for absorption in to the brain, leading to less L-dopa being absorbed.

So although high protein foods are good for naturally increasing L-dopa levels, it is better to eat protein at a different time from when you take Sinemet.

More detail on the biochemistry of Parkinson's Disease :